Analysis of inhibitory mechanisms on Ca^<2+>-dependent K^+ channel influenced by exposure to a time-varying strong magnetic field.

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We tested the effects of exposure to following two magnetic fields (MF) on cultured cells.(a) A time-varying MF changing between 0.07 and 1.7 T at an interval of 3 sec.(b) Extremely-low-frequency (ELF) ME (800 gauss, 50 Hz).(1) Effects of ME (a) on HeLa cells :K^+ uptake was activated and the intracellular Ca^<2+> concentration was increased by replacement of normal medium to high K^+ medium. A membrane-permeable Ca^<2+> chelating agent and Ca^<2+>-dependent K^+ channel inhibitors were found to reduce the K^+ uptake. Exposure to the MF partly inhibited the drug-sensitive K^+ uptake and completely suppressed the increase in intracellular Ca^<2+> in the high K^+ medium. But the inhibition of K^+ uptake by the MF was not restored by addition of Ca^<2+> ionophore. The suppression of K^+ fluxes could relate to a change in electric properties of cell surface and an inhibition of Ca^<2+> influx or Ca^<2+> release from cellular Ca^<2+> stores.(2) Analysis of ELF MF(b) effects on HeLa cells by FT-IR spectra :In analysis of the spectra of the 1500-1700 cm^<-1> region, absorbance of amide II mode (1540 cm-1)was decreased and a band about 1600 cm^<-1> was increased instantly by the MF.Increase in absorbance of the latter band reveals the increase on C=O symmetric vibration of free carboxyl. This results suggest changes in the protein structure of cell membrane and electric properties of cell surface.(3) Effects of ELF MF(a) on bovine adrenal chromaffin cells :We tested the effects of exposure to the time-varying MF(a) on transient increase in intracellular Ca^<2+> stimulated by bradykinin in chromaffin cells. Addition of bradykinin induced the increase in intracellular Ca^<2+> within few minutes.The exposure to the MF perfectly suppressed thc increase in cellular Ca^<2+> in Ca^<2+>-free medium. The inhibition occurred for 15 rain when the maximum magnetic flux density was more than 1.4 T.These results suggest that the exposure inhibits Ca^<2+> release from cellular vesicles.